Thiazide is a term used to describe a type of molecule and a class of diuretic.

The members of this class of diuretics are derived from benzothiadiazine. They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl- symporter. Thiazides also cause loss of potassium and an increase in serum uric acid. The chemical structure of the original thiazide diuretics contained a thiazide ring system; the term is also used for drugs with a similar action that are not chemically thiazides, such as chlortalidone and metolazone, strictly these agents are termed thiazide-like diuretics, but often the term thiazide is used indiscriminately.

That thiazide both refers to the type of molecule and the medication can sometimes lead to confusion, because some molecules (thiazde-like diuretics) are often considered as thiazide diuretics, although they are not thiazides from a chemical perspective. In this context, "thiazide" is taken to refer to a drug which acts at a "thiazide receptor", which is believed to be a sodium-chloride symporter.

Thiazides are often used to treat hypertension, although they are also used to treat congestive heart failure and symptomatic edema. They are the recommended first-line treatment in the US (JNC VII) guidelines and the National Institute for Health and Clinical Excellence/British Hypertension Society guidelines and a recommended treatment in the European (ESC/ESH) guidelines. They have been shown to prevent hypertension-related morbidity and mortality, although how they lower blood pressure in the long term is not fully understood. When administered acutely thiazides lower blood pressure by causing diuresis, a fall in plasma volume and a reduction in cardiac output. However, after chronic use thiazides cause a reduction in blood pressure by lowering peripheral resistance (i.e. vasodilation). The mechanism of this effect is uncertain but it may involve effects on 'whole body' or renal autoregulation, or direct vasodilator actions either through inhibition of carbonic anhydrase or by desensitizing the vascular smooth muscle cells to the rise in intracellular calcium induced by norepinephrine.

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